Production of hydroxyl radicals and their disassociation from myocardial cell injury during calcium paradox

Eddy Duncan, Tomoya Onodera, Muhammad Ashraf

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

The production of hydroxyl radicals during calcium paradox injury was investigated by measuring the production of 2,5-dihydroxybenzoic acid (2,5-DHBA) from salicylate. Four groups of rats were analyzed. In the first group, isolated hearts were perfused with calcium-free medium for 10 minutes followed by perfusion with medium containing Ca++ for 10 minutes. In the other groups, 0.25 μM N,N′-diphenyl-1,3-phenylenediamine (DPPD), 80 μM cytochrome c, or 450 U/ml catalase was added. Coronary effluent was analyzed for the presence of 2,5-DHBA, and tissue sections were examined using light microscopy. In the first group, 2,5-DHBA production began during the calcium-free period, peaked tenfold 60-90 sec. into the Ca repletion period, and declined thereafter. The increase in 2,5-DHBA was accompanied by severe cell damage. Cytochrome c reduced 2,5-DHBA production, and catalase almost completely inhibited 2,5-DHBA production, while DPPD had no effect on 2,5-DHBA production. None of the three additives provided any complete morphological protection. The data provide evidence for the production of hydroxyl radicals during calcium-paradox injury, that their production is dependent upon the presence of hydrogen peroxide, and that cell damage in the calcium paradox is not primarily mediated by the extracellular hydroxyl radicals.

Original languageEnglish (US)
Pages (from-to)11-18
Number of pages8
JournalFree Radical Biology and Medicine
Volume12
Issue number1
DOIs
StatePublished - Jan 1 1992
Externally publishedYes

Fingerprint

Hydroxyl Radical
Calcium
Wounds and Injuries
Cytochromes c
Catalase
Cells
Salicylates
2,5-dihydroxybenzoic acid
Hydrogen Peroxide
Microscopy
Optical microscopy
Perfusion
Rats
Effluents
Light
Tissue

Keywords

  • Calcium paradox
  • Catalase
  • Free radicals
  • HPLC
  • Hydroxyl radical
  • Oxygen-derived radicals
  • Salicylate

ASJC Scopus subject areas

  • Biochemistry
  • Physiology (medical)

Cite this

Production of hydroxyl radicals and their disassociation from myocardial cell injury during calcium paradox. / Duncan, Eddy; Onodera, Tomoya; Ashraf, Muhammad.

In: Free Radical Biology and Medicine, Vol. 12, No. 1, 01.01.1992, p. 11-18.

Research output: Contribution to journalArticle

@article{10021645572f4252a6c49730f505744f,
title = "Production of hydroxyl radicals and their disassociation from myocardial cell injury during calcium paradox",
abstract = "The production of hydroxyl radicals during calcium paradox injury was investigated by measuring the production of 2,5-dihydroxybenzoic acid (2,5-DHBA) from salicylate. Four groups of rats were analyzed. In the first group, isolated hearts were perfused with calcium-free medium for 10 minutes followed by perfusion with medium containing Ca++ for 10 minutes. In the other groups, 0.25 μM N,N′-diphenyl-1,3-phenylenediamine (DPPD), 80 μM cytochrome c, or 450 U/ml catalase was added. Coronary effluent was analyzed for the presence of 2,5-DHBA, and tissue sections were examined using light microscopy. In the first group, 2,5-DHBA production began during the calcium-free period, peaked tenfold 60-90 sec. into the Ca repletion period, and declined thereafter. The increase in 2,5-DHBA was accompanied by severe cell damage. Cytochrome c reduced 2,5-DHBA production, and catalase almost completely inhibited 2,5-DHBA production, while DPPD had no effect on 2,5-DHBA production. None of the three additives provided any complete morphological protection. The data provide evidence for the production of hydroxyl radicals during calcium-paradox injury, that their production is dependent upon the presence of hydrogen peroxide, and that cell damage in the calcium paradox is not primarily mediated by the extracellular hydroxyl radicals.",
keywords = "Calcium paradox, Catalase, Free radicals, HPLC, Hydroxyl radical, Oxygen-derived radicals, Salicylate",
author = "Eddy Duncan and Tomoya Onodera and Muhammad Ashraf",
year = "1992",
month = "1",
day = "1",
doi = "10.1016/0891-5849(92)90053-J",
language = "English (US)",
volume = "12",
pages = "11--18",
journal = "Free Radical Biology and Medicine",
issn = "0891-5849",
publisher = "Elsevier Inc.",
number = "1",

}

TY - JOUR

T1 - Production of hydroxyl radicals and their disassociation from myocardial cell injury during calcium paradox

AU - Duncan, Eddy

AU - Onodera, Tomoya

AU - Ashraf, Muhammad

PY - 1992/1/1

Y1 - 1992/1/1

N2 - The production of hydroxyl radicals during calcium paradox injury was investigated by measuring the production of 2,5-dihydroxybenzoic acid (2,5-DHBA) from salicylate. Four groups of rats were analyzed. In the first group, isolated hearts were perfused with calcium-free medium for 10 minutes followed by perfusion with medium containing Ca++ for 10 minutes. In the other groups, 0.25 μM N,N′-diphenyl-1,3-phenylenediamine (DPPD), 80 μM cytochrome c, or 450 U/ml catalase was added. Coronary effluent was analyzed for the presence of 2,5-DHBA, and tissue sections were examined using light microscopy. In the first group, 2,5-DHBA production began during the calcium-free period, peaked tenfold 60-90 sec. into the Ca repletion period, and declined thereafter. The increase in 2,5-DHBA was accompanied by severe cell damage. Cytochrome c reduced 2,5-DHBA production, and catalase almost completely inhibited 2,5-DHBA production, while DPPD had no effect on 2,5-DHBA production. None of the three additives provided any complete morphological protection. The data provide evidence for the production of hydroxyl radicals during calcium-paradox injury, that their production is dependent upon the presence of hydrogen peroxide, and that cell damage in the calcium paradox is not primarily mediated by the extracellular hydroxyl radicals.

AB - The production of hydroxyl radicals during calcium paradox injury was investigated by measuring the production of 2,5-dihydroxybenzoic acid (2,5-DHBA) from salicylate. Four groups of rats were analyzed. In the first group, isolated hearts were perfused with calcium-free medium for 10 minutes followed by perfusion with medium containing Ca++ for 10 minutes. In the other groups, 0.25 μM N,N′-diphenyl-1,3-phenylenediamine (DPPD), 80 μM cytochrome c, or 450 U/ml catalase was added. Coronary effluent was analyzed for the presence of 2,5-DHBA, and tissue sections were examined using light microscopy. In the first group, 2,5-DHBA production began during the calcium-free period, peaked tenfold 60-90 sec. into the Ca repletion period, and declined thereafter. The increase in 2,5-DHBA was accompanied by severe cell damage. Cytochrome c reduced 2,5-DHBA production, and catalase almost completely inhibited 2,5-DHBA production, while DPPD had no effect on 2,5-DHBA production. None of the three additives provided any complete morphological protection. The data provide evidence for the production of hydroxyl radicals during calcium-paradox injury, that their production is dependent upon the presence of hydrogen peroxide, and that cell damage in the calcium paradox is not primarily mediated by the extracellular hydroxyl radicals.

KW - Calcium paradox

KW - Catalase

KW - Free radicals

KW - HPLC

KW - Hydroxyl radical

KW - Oxygen-derived radicals

KW - Salicylate

UR - http://www.scopus.com/inward/record.url?scp=0026552275&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026552275&partnerID=8YFLogxK

U2 - 10.1016/0891-5849(92)90053-J

DO - 10.1016/0891-5849(92)90053-J

M3 - Article

C2 - 1311280

AN - SCOPUS:0026552275

VL - 12

SP - 11

EP - 18

JO - Free Radical Biology and Medicine

JF - Free Radical Biology and Medicine

SN - 0891-5849

IS - 1

ER -